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Category: genetics

Scientists Discover Dual Treatment for Lung Cancer and Muscle Wasting

Researchers at Oregon State University have pioneered a transformative approach for simultaneously targeting lung cancer and the debilitating muscle-wasting syndrome known as cachexia—a condition that plagues many lung cancer patients. Their groundbreaking work employs lipid nanoparticles (LNPs) as a delivery vehicle for messenger RNA (mRNA) therapeutics, addressing critical challenges in precision drug delivery for aggressive tumors deep within the lung tissue.

Lipid nanoparticles, microscopic carriers composed of fatty compounds like lipids, have revolutionized drug delivery with their ability to ferry genetic material directly into cells. In this study, the OSU team engineered LNPs comprised of DC-cholesterol and a specialized ionizable lipid, 113-O12B, which exhibited a remarkable ability to bind a blood serum protein called vitronectin. This binding triggers the formation of a protein corona on the nanoparticles, a dynamic interface that actively guides the LNPs to lung tissue, and more importantly, lung tumor microenvironments.

Vitronectin’s recruitment is no coincidence. It interacts with integrin receptors—cellular docking proteins highly expressed on lung cancer cells. These integrins act as biological gateways, facilitating enhanced uptake of the therapeutic nanoparticles by tumor cells while sparing healthy tissue. This receptor-mediated targeting marks a significant advance over conventional LNPs, which commonly accumulate in the liver, limiting their therapeutic index against lung malignancies.

10 Enhanced Super-human Types in Frank Herbert’s Dune

Frank Herbert’s Dune saga which has six books in its expanse is no doubt one of the most popular and most influential books in Science fiction. Dune is really about how putting all your hope into a hero or a “chosen one” and then to a set of beliefs can go awry wrong in a big terrifying way. The story shows how easily large groups of people can be influenced by ideas, especially when religion and politics get mixed together, it shows the great game of power on a galactic scale. It showcases how humanity would evolve and transform in the future, some which are familiar while others totally alien in appearance. Then the overall idea of a long “Golden Path” that is meant to ensure the survival of humanity becomes the overarching theme of the saga and along the way, different human types emerge in the storyline, some enhanced by genetic engineering, others by cloning and selective breeding. So, here in this video we will take a look at 10 of these enhanced or superhuman types in the canon Dune works.

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One DNA letter can trigger complete sex reversal

Researchers at Bar-Ilan University have discovered that changing just one letter in DNA can completely alter sex development in mice. In the new study, published in Nature Communications, a single-letter insertion in a non-coding regulatory region caused XX mice, which would normally develop as females, to develop instead as males with testis and male genitalia.

The finding is especially striking because the mutation was not made in a gene itself, but in a distant stretch of DNA that helps control a key developmental gene. The study highlights the major role of the non-coding genome —the 98% of DNA that does not make proteins but helps regulate when and how genes are turned on and off.

“This is a remarkable finding because such a tiny change—just one DNA letter out of approximately 2.8 billion—was enough to produce a dramatic developmental outcome,” said Dr. Nitzan Gonen, from the Goodman Faculty of Life Sciences and Institute of Nanotechnology and Advanced Materials at Bar-Ilan University. “It shows that non-coding DNA can have a profound effect on development and disease.”

We are already gene editing humans

You just haven’t noticed.

George Church, Harvard geneticist and Human Genome Project pioneer, explains why CRISPR wasn’t the real breakthrough, how multiplex gene editing unlocked organ transplants and de-extinction, and why aging will likely require rewriting many genes at once.

Hosted by Mgoes → https://twitter.com/m_goes_distance
Brought to you by SuperHuman Fund → https://superhuman.fund/

0:00 — Gene Editing Mammals → Humans
8:36 — Germline vs Somatic
14:56 — Modified Humans Are Already Here
18:50 — Enhancing Healthy Humans
25:00 — Aging Therapies vs Cognitive Enhancement
30:20 — Embryo Selection
38:10 — Is US Losing To UAE?
42:33 — Biotech Failures
49:31 — Next Dire Wolf Moment
54:21 — AI x Science
1:02:07 — Synthetizing Entire Genomes.

The Accelerate Bio Podcast explores the future of humanity in the age of Artificial Intelligence. Subscribe for deep-dive conversations with founders, scientists, and investors shaping AI, biotechnology, and human progress.

This episode discusses George Church, gene editing, CRISPR, human enhancement, longevity, aging, embryo selection, synthetic biology, multiplex editing, AI biotech.

Continue reading “We are already gene editing humans” | >

Overlooked non-coding genes cause diabetes in babies, study reveals

Scientists have found new genetic causes for diabetes in babies—in a part of the genome that has historically been overlooked in genetic studies. Until recently, most research has investigated causes of disease in “coding” genes—those that produce proteins. Now, academics at the University of Exeter and their international collaborators have found that DNA changes in two genes that instead make functional RNA molecules are a cause of diabetes. RNA plays various roles in the body, including regulating genes and influencing how genetic information is “read” and interpreted.

The study is titled “Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes,” and was published in the American Journal of Human Genetics.

The team used genome sequencing, a method that reads all the letters in a person’s DNA. They found that changes in two genes called RNU4ATAC and RNU6ATAC were the cause of autoimmune neonatal diabetes in 19 children.

Long non-coding RNA may be a promising therapeutic target for cancer

Northwestern Medicine scientists have discovered that a specific long non-coding RNA activates oncogenic signaling pathways in prostate cancer cells and drives tumor progression, underscoring its potential as a therapeutic target, according to a recent study published in Nature Communications. Rendong Yang, Ph.D., associate professor of Urology and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, was co-corresponding author of the study.

Long non-coding RNAs (lncRNAs) are a type of RNA with transcripts that contain more than 200 nucleotides and play a central role in regulating gene expression, most notably in cancer progression. While previous work has identified many cancer-associated lncRNAs, the mechanisms by which lncRNAs influence cancer progression have remained unknown due to lncRNAs’ cell type-specific and tissue-specific gene expression patterns.

In the current study, the scientists aimed to uncover cellular interactions between super-enhancers—clusters of regulatory DNA elements that drive high levels of transcription—and lncRNAs by studying RNA sequencing data from patients with metastatic castration-resistant prostate cancer.

Tau mutation drives autophagy-lysosome dysfunction

The researchers studied a specific mutation in a brain protein called tau that causes the protein to become misfolded and alter its normal function. In general, when tau proteins become misfolded, they build up inside neurons and contribute to various forms of dementia, including Alzheimer’s dementia and frontotemporal dementia, a neurodegenerative disease similar to Alzheimer’s that often strikes earlier — in middle age — and typically involves significant changes in personality and behavior that precede cognitive decline.

In this new study, the researchers studied neurons that had been reprogrammed from skin cells sampled from patients with frontotemporal dementia who carried the tau mutation. In the neurons, the mutated tau proteins caused waste-recycling centers called lysosomes, which are involved in autophagy, to become dysfunctional, allowing cellular waste to accumulate in the lysosomes, which may contribute to neuronal death. The researchers found that enhancing autophagy with an analog of the chemical compound G2 improved clearance of the garbage, reduced tau levels in the lysosomes and prevented cellular toxicity and death.

G2 was discovered in 2019 via screening experiments seeking drugs that could reduce the accumulation of an aggregation-prone protein in a C. elegans model of alpha-1-antitrypsin deficiency, which can cause severe liver disease. The compound was later shown to boost autophagy function in mammalian cell model systems.

The researchers also have shown that G2 can protect brain cells from death in cells modeling Huntington’s disease, a fatal inherited neurodegenerative disease caused by a genetic mutation present at birth. In the cellular model of Huntington’s disease, the compound prevented the buildup of a harmful RNA molecule. ScienceMission sciencenewshighlights.

New research adds to growing evidence that helping brain cells break down and eliminate their own cellular waste is a promising treatment strategy for a variety of neurodegenerative diseases. In lab experiments, the researchers found that exposure to a novel compound can clear a harmful protein from human neurons modeling frontotemporal dementia — a devastating and ultimately fatal condition — and prevent those neurons from dying.

The study is published in the journal Nature Communications.

Continue reading “Tau mutation drives autophagy-lysosome dysfunction” | >

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